Feline Esophagitis Secondary to Gastroesophageal Reflux Disease: Clinical Signs and Radiographic, Endoscopic, and Histopathological Findings
Chronic esophagitis due to gastroesophageal reflux (GER) is rarely reported in the cat. This paper describes the clinical signs and diagnostic findings, including radiographic, endoscopic, and histopathological abnormalities, in three young, purebred, male cats with esophagitis presumed to be secondary to GER. Clinical signs included regurgitation, dysphagia, and weight loss. Contrast radiography revealed GER, esophageal dilatation, and decreased motility. Endoscopy showed hyperemia, increased vascularity, ulcers, erosion, and an abnormal lower esophageal sphincter. Histopathological lesions included squamous hyperplasia and dysplasia, erosions, ulcers, and an inflammatory infiltrate of lymphocytes, plasma cells, and neutrophils. Long-term follow-up demonstrated progression of the disease in two of the cats.
Introduction
Esophagitis secondary to gastroesophageal reflux (GER) is reported in the cat, but little is known about the typical clinical presentation, diagnostic findings, and course of the disease. The incidence of reflux esophagitis in the cat is thought to be low, but infrequent diagnosis may be due to poor understanding of the syndrome rather than rare occurrence.1 Esophagitis can be associated with many underlying causes, such as foreign bodies, neoplasia, ingested toxins or medications, iatrogenic causes, and postanesthetic reflux; but esophagitis secondary to GER is discussed in a very limited fashion in the veterinary literature.2–6 This paper describes the clinical signs and diagnostic findings (including radiographic, endoscopic, and histopathological abnormalities in three cats with esophagitis believed to be secondary to GER) and also looks at the medical literature to try to better characterize this syndrome in cats.
Case Reports
Case No. 1
A 2-year-old, neutered male, exotic shorthair cat was referred for management of previously diagnosed esophagitis, mild gastroenteritis, intermittent vomiting, and vocalizing as though in pain. Twenty-one months prior to referral, the patient underwent endoscopy for chronic vomiting, regurgitation, and vocalizing at the age of 3 months. Routine blood work was unremarkable at that time. Endoscopy revealed a hyperemic, proliferative, irregular esophagus and a grossly normal stomach and duodenum. The esophageal mucosa was ulcerated with severe infiltration of neutrophils, lymphocytes, and plasma cells. The remaining squamous epithelium was moderately hyperplastic. The gastric and intestinal biopsies were compatible with a mild gastroenteritis with spiral bacteria seen. The patient was treated with various combinations of acid blockers, prokinetic agents, and antibiotics.
Nine months later, the patient still experienced bouts of vomiting and regurgitation and episodes of vocalization. Blood work, urinalysis, and survey thoracic and abdominal radiographs were unremarkable. A contrast esophageal radiograph showed poor esophageal motility. An acetylcholine receptor antibody titer was 0.0 nmol/L (reference range, <0.3 nmol/L). Oral corticosteroids were added to the therapy by the referring veterinarian prior to referral.
The patient was referred to the Animal Medical Center (AMC) 2 years after initial diagnostics, because the signs had progressed to intermittent vomiting every 3 to 4 days, a decreased appetite for 2 to 3 days, and weight loss of 0.35 kg over the last 9 months. Current medications were famotidine and an anti-inflammatory dose of prednisone. Physical examination, complete blood count (CBC), and serum biochemical profile were unremarkable. The patient was negative for feline leukemia and feline immunodeficiency viruses based on enzyme-linked immunosorbent assay (ELISA) testing. Thoracic and abdominal radiographs were repeated and considered unremarkable. A contrast esophageal and gastrointestinal (GI) series showed mild dilatation of the esophagus and GER at 10 and 20 minutes. Fluoroscopy was only performed in the initial few minutes of the esophagram. The remainder of the GI series was unremarkable.
The patient was anesthetized with ketamine and Valium and maintained on isoflurane. Endoscopy showed the distal third of the esophagus to be dilated, hyperemic, and irregular, with multiple polyploid masses. The area of the esophageal sphincter had multiple cystic masses. The lower esophageal sphincter (LES) was irregularly shaped and dilated [Figure 1]. The stomach had two polyploid masses on the gastric side of the cardiac sphincter. The cardia and fundus were normal. The pylorus had two polyploid masses attached to the sphincter. The duodenum appeared normal. Biopsies were taken of the distal esophagus. Biopsies of both the cystic masses and the more diffuse, hyperemic, irregular areas of the esophagus were taken with an aspiration capsule instrument.a Biopsies of the cardia, fundus, duodenum, and pyloric masses were taken with standard, flexible, endoscopic biopsy instruments.
Results of histopathology of the esophagus and mass-like areas showed multifocally eroded and hyperplastic epithelium of the mucosa. The submucosa contained an inflammatory infiltrate of lymphocytes, plasma cells, and neutrophils. The gastric and duodenal biopsies were unremarkable. No spiral bacteria were seen, perhaps because of the previous therapy. The client was instructed to discontinue the prednisone, because there was no evidence of a primary immune or inflammatory disorder; and instructions were given to continue the famotidine and add the prokinetic cisapride indefinitely, depending on clinical signs and reevaluation.
The patient was seen for reevaluation 1 year and 5 months later, and he was doing well. He still had bouts of regurgitation, vomiting, and inappetence that lasted 3 to 4 days, every 1 to 2 months. His weight was stable, and physical examination was unremarkable. He was switched to the proton pump inhibitor omeprazole in place of the famotidine to see if clinical signs would improve with a different antacid. Communication with the owner over the following 21 months revealed the patient was doing clinically well. Twenty-one months later, the owners agreed to allow another contrast esophageal radiograph and endoscopic procedure to evaluate the esophagus and assess disease progression. Survey thoracic radiographs were unremarkable. A fluoroscopic barium esophageal study showed a mildly dilated distal esophagus and decreased esophageal motility, both of which appeared to be unchanged from the previous evaluation 21 months earlier.
The patient was anesthetized with ketamine and Valium and maintained on isoflurane for endoscopic evaluation. Endoscopy revealed the esophagus was extremely hyperemic and edematous with diffuse, multiple, polyploid masses in the distal third [Figure 2]. There was a marked exaggeration of the normal striations in the esophagus, with polyploid masses protruding from them. The LES was mildly dilated. The stomach was grossly normal, the masses previously seen at the pylorus were absent, and the duodenum was slightly pale and mottled. Biopsies were taken with standard, flexible, endoscopic biopsy instruments. In addition, biopsies of the esophagus were also taken with an aspiration capsule.
Histopathology of the esophagus revealed marked, irregular, mucosal squamous epithelial hyperplasia [Figure 3]. There were areas of focal papillary projections. There were areas of superficial erosion with moderate infiltrates of mixed inflammatory cells [Figure 4]. The submucosa contained moderate to focally marked infiltrates of mixed inflammatory cells, of which lymphocytes and plasma cells were dominant. The stomach and duodenum showed no significant lesions. The diagnosis was marked, chronic, proliferative esophagitis. Upon further questioning, the owners revealed that they maintained the cat on famotidine and cisapride, and only when the bouts were more frequent or severe did they change to the omeprazole. The clients were instructed to continue therapy with the omeprazole, since the cat seemed to be more responsive to that medication. Follow-up showed an improvement in the clinical signs, with bouts of regurgitation and vomiting only occurring about every 2 weeks.
Case No. 2
A 5-month-old, intact male, oriental shorthair cat was referred to the AMC for regurgitation that started when the kitten began eating solid food, and a presumptive diagnosis of megaesophagus, although no imaging had been performed. Blood work results from 2 months prior, performed by the referring veterinarian, were unremarkable. The kitten was otherwise active and playful, and there was no coughing or respiratory problems. Regurgitation seemed to occur when the kitten was active, and it was preceded by licking of the lips and retching. Physical examination was unremarkable. The patient was admitted for radiographs, contrast esophageal and GI series, and endoscopy. Survey thoracic and abdominal radiographs were unremarkable. The contrast esophageal and GI series showed decreased esophageal motility and mild dilatation with GER at 10, 20, and 30 minutes after barium administration. Fluoroscopy was performed only for the first few minutes for the initial evaluation of esophageal motility. The remainder of the GI series was normal.
The patient was anesthetized with ketamine and Valium and maintained on isoflurane for endoscopic evaluation. Endoscopy revealed that the esophagus was mildly distended with mild accumulation of fluid. The gastro-esophageal junction was very dilated, and no discernible LES was seen. There were multiple new and old ulcerations noted in the distal esophagus. The stomach appeared grossly normal. Unfortunately, no biopsies were taken. The diagnosis was an abnormality of the LES with GER and esophagitis and decreased esophageal motility. The patient was treated with famotidine, sucralfate, and cisapride. The owner was instructed to administer the sucralfate at least 2 hours apart from other medications.
The patient was reevaluated 5 months later. He was doing well and having about one episode of regurgitation per week and licking his lips as if nauseous about three to four times per week. His weight was stable, and physical examination was unremarkable. The owner had discontinued the sucralfate after the initial 1 month and did not feel that the clinical signs worsened afterward. The owner was instructed to continue the famotidine and cisapride.
The patient was seen 8 months later (1 year, 1 month after initial presentation). Physical examination was unremarkable. He was still having waxing and waning bouts of regurgitation and periods of seeming to be in pain (vocalizing and acting restless and uncomfortable). Otherwise, appetite and activity levels were normal, and there were no respiratory signs. The owner declined a follow-up endoscopy and contrast esophageal radiography at this time. The episodes of discomfort were attributed to GER, and the owner was instructed to continue the cisapride, discontinue the famotidine, and start omeprazole as the antacid to see if a different type of antacid was more effective in controlling the clinical signs.
The patient was not seen at the AMC until 2 years later. He had been stable with his signs until 2 to 3 months prior to this visit. His appetite had been increased for 2 to 3 months, and he was vomiting about two times per day for the last month. Blood work, trypsin-like immunoreactivity/ folate/cobalamine levels, and thoracic radiography were performed. Endoscopy with biopsies was also repeated to assess condition status.
The blood work was unremarkable. Thoracic radiographs revealed the development of a megaesophagus. Endoscopy showed the esophagus was dilated throughout the cervical and thoracic regions. The distal esophagus no longer had significant gross mucosal hyperplasia. The LES appeared absent as before. There were a few areas of erosion in the thoracic esophagus. The duodenum, cardia, and pylorus appeared grossly normal. Biopsies of all areas were taken, with additional pieces of the esophagus biopsied with the aspiration capsule.
Histopathology of the esophagus showed moderate to marked squamous hyperplasia with moderate submucosal infiltration by mixed inflammatory cells (predominantly plasma cells and lymphocytes, with fewer neutrophils). There were some areas of squamous dysplasia [Figures 5, 6]. The gastric biopsies revealed moderate, multifocal, mucosal infiltration of mixed inflammatory cells (predominantly lymphocytes with fewer plasma cells). There were also moderate numbers of helical bacteria seen on the mucosal surfaces of many sections. The diagnosis was moderate, chronic, active, hyperplastic esophagitis and a moderate Helicobacter-associated gastritis.
The patient was discharged with the same medications as before, with the addition of clarithromycin to treat the Helicobacter infection. Instructions were given to the owner to feed the patient in an upright position because of the megaesophagus. At follow-up, the cat’s condition was deemed stable.
Case No. 3
A 2-year-old, neutered male, Egyptian mau cat was referred to the AMC for gagging and dysphagia while eating soft food, and regurgitating soon after eating hard food. The owner also perceived that the cat was in discomfort after eating. These signs had been present since the pet had been adopted from a shelter 5 months prior. Physical examination revealed slightly irregular, small kidneys. Survey thoracic and abdominal radiographs revealed slightly small kidneys.
The patient was admitted to the hospital for endoscopy. The patient was anesthetized with ketamine and Valium and maintained on isoflurane. The distal third of the esophagus was very irregular and proliferative, with exaggeration of the mucosal striations, and the LES was dilated. The stomach was smooth and friable. The duodenum could not be visualized, and biopsies were obtained blindly. Tissue from the esophagus was obtained with an aspiration capsule, and tissue from the stomach and duodenum was obtained with a standard, flexible, endoscopic biopsy instrument. Tissues were submitted for histopathological evaluation. Cytopathology of the pylorus revealed spiral bacteria. The patient was discharged with famotidine, doxycycline, and cisapride. The doxycycline was administered for 3 weeks, while the other medications were lifelong.
Histopathology revealed focal, lymphocytic gastritis; moderate, lymphocytic enteritis; severe, squamous hyperplasia; and moderate, submucosal inflammation, consistent with chronic esophagitis. No spiral bacteria were noted. The owner was instructed to continue the famotidine, and an elimination diet of lamb and rice was instituted. The cat did very well while on this regimen, with almost complete resolution of clinical signs, but he would relapse if any of the medications were discontinued. Although contrast radiography was not performed, the authors feel that this case was similar to the two others and should be included as a probable case of esophagitis secondary to GER.
Discussion
A review of the veterinary literature yielded only two papers about reflux esophagitis in cats. The first paper was a case of a 1-year-old, neutered female domestic shorthair that presented for chronic upper respiratory infections, anorexia, and swallowing and gagging as if it had a “bone stuck in its throat.”7 Limited diagnostics were performed, and no treatment was attempted. The patient was diagnosed with chronic esophagitis secondary to GER, based on necropsy.
The second paper discussed two cases of cats with esophagitis thought to be secondary to GER.8 These were similar to the cases in this report, in that the cats were young, purebred, male cats with structurally and histopathologically similar lesions and similar presenting clinical signs. The first case was a 13-month-old, intact male Russian blue cat that presented for emaciation and chronic, intermittent vomiting that usually occurred immediately postprandial. The second case from that study was a 9-month-old, intact Siamese cat that presented for 4 months of regurgitation and weight loss.
Esophagitis and esophageal stricture formation secondary to reflux during or postanesthesia in two cats have been described, yielding useful information about the clinical signs of esophagitis and the abnormalities seen on radiography, endoscopy, and histopathology.9 The major clinical signs were regurgitation and dysphagia postanesthesia. Ptyalism, coughing, and weight loss were also seen. Radiographs of the neck and thorax were normal. Segmental narrowing of the esophageal lumen was demonstrated after administration of barium. Endoscopy showed hyperemia and mucosal ulceration of the esophagus and visualization of the stricture. Histopathological changes in these cases showed loss of esophageal epithelium, and granulation and connective tissue extending from the base of the ulcer into the esophageal muscle.
Cats are used as a model for human esophagitis, and there are various studies in the human medical literature describing histopathological changes seen in experimentally induced esophagitis.10–13 A study by Dodds, et al., looked at radiographic and histopathological changes in cats with varying degrees of experimentally induced esophagitis.10 The study revealed that esophagitis limited to the mucosal layer did not show abnormalities on contrast esophageal radiography. However, if the inflammatory phase of esophagitis extended into the submucosa or sub-mucosa and muscularis, esophagrams usually showed luminal narrowing. Mucosal ulcerations were not visualized on contrast esophageal radiography. Histopathology showed acute esophagitis in these cases, characterized by edema, vascular engorgement, and a polymorphonuclear infiltrate of varying degree and depth, depending on the severity of the insult. Since these patients were subjected to only a single insult and then euthanized, there were no descriptions of changes seen with chronic esophagitis. Esophageal motility was not assessed in that study. A paper by Geisinger, et al., showed that in experimentally induced esophagitis in cats, basal cell hyperplasia was the most sensitive marker of acid injury, followed by intraepithelial leukocytes, subepithelial leukocyte infiltration, and ulceration.11
These cases illustrate the clinical syndrome of chronic esophagitis believed to be secondary to GER in cats. The “gold standard” for diagnosing GER in humans is 24-hour ambulatory esophageal pH monitoring.12 However, it is still primarily diagnosed in humans based on clinical signs and history. Esophageal pH monitoring is not readily available for animal patients; thus, diagnoses in the cases of this study were made based on similarities of history, clinical signs, and radiographic, endoscopic, and histopathological findings. Historically, esophagitis and GER are poorly characterized in cats, and the incidence is thought to be low.1 Esophagitis should be considered in any cat that presents for vomiting, regurgitation, and dysphagia. It is imperative to carefully question owners, as most owners do not know how to distinguish between vomiting and regurgitation. Other clinical signs sometimes seen are coughing from aspiration of refluxed material, licking of lips, repeated swallowing motions, discomfort, ptyalism, lethargy, and weight loss.
Radiology is useful in assessing for structural issues such as foreign bodies, strictures, hernias, and intussusceptions.14 Contrast radiography can also be used to assess esophageal motility and GER. The limitation of radiography is inadequate mucosal assessment. There is no gross or microscopic assessment of the mucosa, and it is very insensitive in the detection of ulcers and erosions.10 When reflux esophagitis is suspected, the value of plain radiographs should not be overlooked, as these can eliminate underlying causes such as foreign bodies, neoplasia, and megaesophagus. Contrast radiography of the esophagus and upper GI tract is important to assess motility issues in the esophagus. It can also elucidate structural issues such as strictures that are not seen on plain radiography. An upper GI series can assess for concurrent GI disease and GI issues such as masses, delayed gastric emptying, or structural abnormalities that predispose to reflux and esophagitis. In the authors’ review of the literature and the cases of this study, plain radiographs were usually unremarkable, although a megaesophagus was seen in case no. 2 of this study as the esophageal disease progressed. Contrast radiography was useful in assessing GER, retention of barium in the esophagus, segmental dilatation of the esophagus, and prominent mucosal striations presumed to correlate with mucosal hyperplasia. Of these, the most consistent finding was GER in the cases of this study and in the cases in Lobetti, et al.’s, paper.8 Gastroesophageal reflux can be seen in animals without disease, so the significance of it should be taken into context with clinical signs and pathological findings. Segmental dilatation tended to be in the distal esophagus. Luminal narrowing, as described by Dodds, et al., was not seen in the cases of this study, perhaps because all of the cases in Dodds’ study were acute insults, whereas the cases in this study were chronic.10
Endoscopy is usually the next step in assessing esophagitis. Endoscopy enables the clinician to visualize structural abnormalities as well as the gross appearance of the esophageal mucosa and to obtain biopsies. However, it is poor at evaluating esophageal motility. Endoscopy is always done under general anesthesia, and anesthetic effects on the esophageal examination must be taken into consideration. Agents known to decrease lower esophageal pressure include diazepam, atropine, morphine, xylazine, and acepromazine.1516
A dilated LES in an anesthetized animal may be considered normal in the absence of clinical signs and other gross abnormalities. The LES lies at the level of the diaphragm and courses ventrally after passing through the hiatus. This area of increased pressure between the esophagus and stomach maintains unidirectional flow of food and liquid and prevents reflux. In cats, the LES is composed of smooth muscle that responds to vagal and nonvagal stimulation via alpha-adrenergic and cholinergic receptors.17–19 During swallowing, there is a vagally mediated relaxation of the LES beginning about 5 seconds before a food bolus reaches the sphincter, which then opens and allows the food to pass. In addition to the physiological control of the LES, there are anatomical structures that enhance LES tone and pressure. The diaphragm contributes to LES competence by maintaining an oblique entry of the esophagus into the stomach. Crural myotomy in cats increases the frequency of GER.20 Also, when a meal is ingested, gastric distension causes the angle at which the esophagus enters the stomach to become more oblique, thus decreasing the chance of reflux, and also causes compression of the LES by the distended fundus. Mucosal folds of the cardia and the phreno-esophageal membrane are anatomical structures that help maintain closure of the LES. In the cats of this study and in Lobetti, et al’s, cats, LES incompetence or malformation appeared to be the cause of GER.8
In the cases discussed here, the typical gross abnormalities seen with chronic esophagitis are distal esophageal erythema and hyperemia, erosion, ulceration, or increased vascularity. Distal esophageal mucosal hyperplasia evidenced by exaggeration of striations, polyploid growths, and a dilated LES were also seen. The significance of a dilated LES is questionable since these animals were anesthetized, but a dilated LES was present in the cases presented here and in Lobetti, et al.’s, cases. The two patients in Lobetti, et al.’s, paper were anesthetized with an agent that maintains LES pressure better than other agents.821 An abnormally shaped or dilated LES may also be seen.
Despite all of these changes commonly seen with chronic esophagitis, it cannot be ruled out based on normal gross appearance, because esophagitis can be present despite a grossly normal-appearing mucosa. In the human condition of a ringed or corrugated esophagus, the patient has a series of concentric rings in the esophagus with normal-appearing mucosa.22 But in one study, 11 out of 11 patients having a ringed esophagus with normal-looking mucosa had histopathological changes consistent with esophagitis.22 In a study by Dodds, et al., cats that received a single acid insult to the esophagus had esophageal mucosa that appeared normal during the reparative phase, while there was histopathological evidence of esophagitis in five of six cats that were euthanized 1 week following insult, in three of four cats 2 weeks following insult, and in two of four cats 4 weeks following insult.10 In one of Lobetti, et al.’s cases, the esophagus was grossly normal on necropsy, but there was histopathological evidence of esophagitis.8
Biopsy of the esophagus is often not performed because of the difficulty in obtaining samples. It is virtually impossible to obtain adequate samples of the esophagus with the typical flexible endoscopic instruments, except in the most severe cases of esophagitis. Mucosal biopsy requires the use of an aspiration capsule biopsy instrument or a rigid biopsy instrument such as a Jackson Forceps. All lesions should be biopsied as well as the distal esophagus in animals with clinical signs of esophageal disease. Findings on histopathological examination, based on the cases of this study and cases of experimentally induced esophagitis, include squamous cell hyperplasia or dysplasia, erosions, ulcers, and inflammatory infiltrates of lymphocytes and plasma cells, with neutrophils in the more acute phases.1011
Treatment is extrapolated from the human literature and will be discussed only briefly because of the lack of cases seen clinically and in the literature and the lack of long-term assessment in most cases. Treatment is aimed at decreasing the amount and frequency of reflux, changing the composition of refluxed material, protecting the esophagus, and healing any existing ulcers or erosion.23–32 Surgical treatment is reserved for cases that fail to respond to medical therapy and is rarely pursued in veterinary patients.3334
As the veterinary community identifies and continues to monitor these cases, information about treatment and long-term prognosis can be garnered. It is interesting to note that one of the cases of this report exhibited squamous dysplasia. In humans, intestinal metaplasia with columnar epithelium in the esophagus (i.e., Barret’s esophagus) is considered a precancerous condition. Since squamous cell carcinoma is the most common neoplasia seen in the feline esophagus, it would be interesting to see if this cat from this study eventually develops esophageal squamous cell carcinoma, or if cats diagnosed with esophageal squamous cell carcinoma retrospectively had chronic clinical signs of esophagitis. It is also interesting to note that the cats of this study and the cases described by Lobetti, et al., that were diagnosed with esophagitis secondary to GER were all young, male, purebred cats; although again, this number is too small to determine if there is a true breed or sex predisposition.8 However, the authors do know that there are breed predispositions for other congenital esophageal disorders, such as hiatal hernias in the Chinese shar pei and megaesophagus in cats.3536
Conclusion
The authors believe that these cases support the existence of chronic esophagitis secondary to GER in cats. Infrequent diagnosis may be due to poor understanding of the syndrome rather than rare occurrence. Criteria for diagnosing esophagitis include clinical signs such as regurgitation, dysphagia, ptyalism, anorexia, weight loss, and respiratory signs. Contrast esophageal radiography may show GER, esophageal dilatation, and decreased motility. Endoscopy may reveal hyperemia, increased vascularity, ulcers, erosions, mucosal hyperplasia, and a dilated or abnormal LES, or the esophagus may appear grossly normal. Histopathological lesions include squamous hyperplasia and dysplasia, erosions, ulcers, and an inflammatory infiltrate of primarily lymphocytes and plasmacytes, with neutrophils in the more acute phases. Treatment consists of acid blockers, prokinetic agents, and cytoprotective agents.
Multipurpose Suction Biopsy Tube, Model 4.7 mm × 120 cm; Quinton Instruments, Seattle, WA
Citation: Journal of the American Animal Hospital Association 39, 2; 10.5326/0390161
Citation: Journal of the American Animal Hospital Association 39, 2; 10.5326/0390161
Citation: Journal of the American Animal Hospital Association 39, 2; 10.5326/0390161
Citation: Journal of the American Animal Hospital Association 39, 2; 10.5326/0390161
Citation: Journal of the American Animal Hospital Association 39, 2; 10.5326/0390161
Citation: Journal of the American Animal Hospital Association 39, 2; 10.5326/0390161
Endoscopic image of the irregularly shaped lower esophageal sphincter in a 2-year-old, exotic shorthair cat with a history of chronic vomiting and regurgitation (case no. 1).
Histopathology of the esophagus illustrating squamous hyperplasia in case no. 1 (Hematoxylin and eosin stain, 200×; bar=50 μm).
Histopathology illustrating erosion at the junction of the lower esophageal sphincter and the cardia in case no. 1 (Hematoxylin and eosin stain, 200×; bar=50 μm).
Histopathology of the esophagus illustrating squamous dysplasia in case no. 2. The lower half of the epithelium is poorly organized, and there is loss of cellular polarity. The arrow denotes mitotic figures (Hematoxylin and eosin stain, 200×; bar=50 μm).
Histopathology of normal feline esophagus (Hematoxylin and eosin stain, 200×; bar=50 μm).
Contributor Notes
